2014 Hypertens Pregnancy, 2014; 33(2): 177–190 ! Informa Healthcare USA, Inc. ISSN: 1064-1955 print / 1525-6065 online DOI: 10.3109/10641955.2013.846368 ORIGINAL ARTICLE Bradykinin B 1 receptor-mediated vasodilation is impaired in myometrial arteries from women with pre-eclampsia Amie J. Moyes, 1,2 Gillan A. Gray, 2 and Fiona C. Denison 1 1 Centre for Reproductive Biology and 2 Centre for Cardiovascular Science, Queens Medical Research Institute, University of Edinburgh, Edinburgh, UK Objective: To investigate the vascular functional activity, localisation and expression of B 1 and B 2 kinin receptors in normal pregnancy and pre-eclampsia. Methods: Kinin receptor-mediated relaxation of myometrial arteries was assessed using wire myography. Immunohistochemical staining and gene expression of kinin receptors in the myometrium was determined. Results: B 2 receptor-mediated relaxation was reduced in pre-eclampsia. B 1 receptor-mediated relaxation was observed in a proportion of healthy women and was impaired in pre-eclampsia. Receptor expression and localisation was unaltered in pre-eclampsia. Conclusion: Here, we demonstrate a novel B 1 receptor-mediated vasodilatation in healthy myometrial vessels that is absent in pre- eclampsia. Keywords Endothelium, Kinin, Myometrium, Pregnancy, Pre-eclampsia. INTRODUCTION Pre-eclampsia is a pregnancy-related disease characterised by hypertension and proteinuria. A common pathological feature of pre-eclampsia is maternal and placental endothelial dysfunction (1). The endothelium plays a funda- mental role in pregnancy, altering the production of vasoactive mediators to regulate vascular tone and blood flow to the uterus and fetoplacental unit (2). These vascular adaptations are vital for a successful pregnancy and it is widely believed that disturbances of, or damage to the endothelium is involved in the development of pre-eclampsia (3,4). There is overwhelming evidence to support this theory including alterations of circulating markers in the plasma from pre-eclamptic women such as a decrease of vasodilatory prostacyclin (5), an increase in thromboxane, endothelin (6), von Willebrand factor (7), and an increase in sensitivity to angiotensin II (8). Functional studies of isolated vessels from women with pre-eclampsia have provided further evidence of impaired endothelial function in the maternal vasculature. Attenuated Correspondence: Dr. Amie Moyes, Cardiovascular Pharmacology, William Harvey Heart Centre, Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, UK. Tel: +44 (0)20 7882 5780. E-mail: a.j.moyes@qmul.ac.uk